In a general manner, the respiratory pathology known as “Sleep Apnea Syndrome” (SAS) is characterized by the frequent occurrence (at least 10 to 20 times per hour) of apneae during a sleep phase of the patient. An “apnea” (or respiratory pause) is defined as a temporary stop of the respiratory function, with a duration longer than 10 seconds. SAS can also be characterized by the occurrence of hypopneae under the same conditions. A “hypopnea” is defined as a significant decrease (but with no interruption) of breathing airflow, typically a decrease of more than 50% compared to an average of the preceding air flow.
Facing this pathology, that concerns more than 4% of the population, and more than 50% of the patients suffering from heart failure, the autonomic nervous system adapts, but with a noxious effect on sleep, to the interruption or reduction of breathing airflow leading to a decrease of the blood oxygen concentration, as well as unconscious micro-awakenings. That is followed, during arousal, by diurnal sleepiness with a loss of attention and increased risks of road accidents. Moreover, the physiologic, then pathologic, adaptive response of certain organs, including the heart and respiratory system, leads to a greater incidence of disorders such as arterial hypertension, ventricular arrhythmiae, myocardial infarction and heart failure.
Diverse techniques intended to detect sleep respiratory disorders by means of an implantable device are known in the prior art. For example, European patent EP 0970713 and its U.S. patent counterpart U.S. Pat. No. 6,574,507 (commonly assigned herewith to ELA Medical) discloses a device that diagnoses the occurrence of an apnea based upon a signal representing minute ventilation (VE signal, or MV signal). Minute ventilation is a parameter that is preponderantly physiological in nature, usually obtained through a measurement of a transthoracic impedance, providing a continuous indication of the patient's respiratory rhythm. This measurement of minute ventilation is performed by injecting current pulses between two electrodes positioned within the thoracic cage, or between the case of the implanted device and an electrode, for example, a pacing electrode and measuring the impedance based on the voltage as a function of the current input. The variations of impedance are correlated with the variations of thoracic volume, with peaks of impedance during inspiration, when the lungs are filled with air, and a decreasing impedance during the expiratory phase.
However, it has been observed in the field, within clinical studies, that this technique for measuring respiratory activity by recording the variations of pulmonary volume at the thoracic level may be susceptible, under certain circumstances, to the detection of false positives and false negatives that are likely to interfere with the accurate interpretation of the signals by the device.
Thus, the transthoracic impedance is varying as a function of the resistivity of the tissues at the moment when current pulse is injected; as this resistivity mainly depends on the air quantity in the lungs, and quantity of blood in heart cavities, the collected impedance signal is modulated by the respiration and heart rate. The impedance is also modulated by the variations of the distance between the measurement electrode and the device's case, a distance that is varying as a function of heart beats. Also, the respiratory component of the signal (its dynamic variation, being the only significant parameter) is added to a static component, relating to the impedance of the tissues when in stable body position, and in the absence of respiration and heart beat.
Thus, the transthoracic impedance can be modified by the patient's movements, or can vary due to the effect of diaphragmatic contractions during an obstructive apnea. These phenomena are inducing artifacts that interfere with the system, and may lead to an erroneous detection of particularly large or fast respiratory cycles, or on the contrary respiratory cycles of low amplitude and/or long period, possibly leading to false positives.
Another type of artifact may result from the presence as part of the impedance signal, of a component relating to heart beats. Indeed, under certain circumstances (for example, in situations of both bradycardia and hyperventilation), the respiratory rate and heart rate may become enough close to each other, so that the heart beats significantly influence the impedance signal. The heart rhythm may therefore be misinterpreted as a respiratory rhythm, with a risk to hide the presence of an apnea or hypopnea (false negative, at the moment when a true pathologic respiratory event occurs).
Ideally, in order to diagnose a respiratory sleep disorder, while avoiding the drawbacks of transthoracic impedance measurement, the best criterion would be a measurement of oxygen saturation in blood, the diagnosis of SAS being confirmed only in cases of confirmed and significant desaturation.
Indeed, the patients suffering from apneae or hypopneae present cyclic variations of heart rate and arterial pressure, indeed at the moment of micro-awakening and ventilatory recovery that follow the apnea, an adrenergic reaction occurs, inducing a tachycardia and an increase of heart flow that therefore compensate the hypoxemia induced by the apnea, in such a manner that, by reaction, the blood is maintained at the same level of oxygen saturation. However that direct measurement is difficult to realize in a simple and permanent way, as part of an implanted device.